Toxicological Effects of Trichloroethylene Exposure

Trichloroethylene (TCE) is a volatile organic solvent extensively employed in degreasing, dry cleaning and chemical synthesis. Environmental and occupational exposures occur predominantly via inhalation, dermal contact and ingestion of contaminated water. Once absorbed, TCE undergoes biotransformation through cytochrome P450-dependent oxidation and glutathione conjugation pathways, yielding reactive intermediates that selectively accumulate in the liver, kidney and central nervous system. Epidemiological and experimental evidence establishes TCE as a human carcinogen, with strongest associations for kidney cancer and suggestive links to liver cancer and non-Hodgkin lymphoma. Non-cancer effects include neurotoxicity manifesting as cognitive and motor deficits, immune dysregulation leading to hypersensitivity dermatitis and autoimmune phenomena, and developmental cardiotoxicity. Mechanistic studies highlight roles for oxidative stress, genotoxicity, impaired mitochondrial function and iron-dependent cell death (ferroptosis). Globally, TCE contamination of groundwater and indoor air remains a public health concern, driving advances in probabilistic risk assessment, biomonitoring programmes and remediation technologies.

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Toxicological Effects of Trichloroethylene Exposure publication trend

The graph below shows the total number of articles in toxicological effects of trichloroethylene exposure across all publications each year (not limited to Nature Index journals).

Technical terms

Carcinogenicity: The ability of a substance to cause cancer by inducing genetic or epigenetic alterations in cells.

Ferroptosis: A regulated form of cell death driven by iron-dependent lipid peroxidation and characterised by mitochondrial shrinkage and membrane damage.

C5b-9 membrane attack complex: A terminal assembly of the complement cascade that forms pores in cell membranes, leading to cell lysis or sublethal signalling.

Mitochondrial permeability transition pore: A non-specific channel in the inner mitochondrial membrane whose prolonged opening disrupts membrane potential and can trigger cell death.

Toxicokinetics: The study of absorption, distribution, metabolism and excretion of chemicals, determining internal dose and variability across populations.

References

1. IP3R-dependent mitochondrial dysfunction mediates C5b-9-induced ferroptosis in trichloroethylene-caused immune kidney injury. Frontiers in Immunology (2023).
2. Human Health Effects of Trichloroethylene: Key Findings and Scientific Issues. Environmental Health Perspectives (2012).
3. Metabolism of trichloroethylene.. Environmental Health Perspectives (2000).
4. Evidence of Autoimmune-Related Effects of Trichloroethylene Exposure from Studies in Mice and Humans. Environmental Health Perspectives (2009).
5. Physiologically Based Pharmacokinetic (PBPK) Modeling of Interstrain Variability in Trichloroethylene Metabolism in the Mouse. Environmental Health Perspectives (2014).
6. Trichloroethylene and Cancer: Systematic and Quantitative Review of Epidemiologic Evidence for Identifying Hazards. International Journal of Environmental Research and Public Health (2011).